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Elevated triglycerides may contribute to atherosclerosis and are a component of metabolic syndrome. They are often elevated alongside insulin resistance. Consult your healthcare provider.

Of all the values in a lipid panel, LDL has the strongest causal link with atherosclerosis. Every LDL particle carries one apolipoprotein B, enters the artery wall and can lodge there. The more of those particles pass through over decades, the more plaque builds up. That is why lowering a raised LDL is the best-evidenced way to reduce the risk of a heart attack and a stroke. The most important sentence on this page, however, is not about high or low but about for whom. The 3.0 mmol/l upper limit on your report is a reference interval: it describes what is common in the population. It is not a goal. Guidelines tie the goal to your risk. <table><thead><tr><th>Situation</th><th>Guideline LDL goal</th></tr></thead><tbody><tr><td>Established cardiovascular disease, up to age 70 (Dutch CVRM guideline)</td><td>below 1.8 mmol/l</td></tr><tr><td>High or very high risk, or diabetes or chronic kidney disease, up to age 70 (CVRM)</td><td>below 2.6 mmol/l</td></tr><tr><td>Very high risk (ESC/EAS 2019)</td><td>below 1.4 mmol/l</td></tr><tr><td>High risk (ESC/EAS 2019)</td><td>below 1.8 mmol/l</td></tr><tr><td>Moderate risk (ESC/EAS 2019)</td><td>below 2.6 mmol/l</td></tr><tr><td>Low risk (ESC/EAS 2019)</td><td>below 3.0 mmol/l</td></tr></tbody></table> The consequence is sharp. An LDL of 2.8 mmol/l sits neatly inside the reference interval on the printout, while that same 2.8 is clearly too high for someone who has had a heart attack. Conversely, an LDL of 3.2 in a thirty-year-old with no other risk factors leads to a very different conversation than in a sixty-year-old who smokes, has diabetes and has high blood pressure. Your risk category, built from age, blood pressure, smoking, diabetes, kidney function, family history and existing cardiovascular disease, is what decides what your number means. Above seventy, LDL lowering is not routinely started in people without cardiovascular disease. A second situation deserves attention. A strongly raised LDL in someone who takes no lipid-lowering medication, particularly alongside early cardiovascular disease in close relatives, is a reason for a doctor to look into whether familial hypercholesterolaemia may be present. That inherited condition affects roughly 1 in 250 to 300 people and remains under-diagnosed in the Netherlands. A blood value does not make that diagnosis and cannot make it: the conversation belongs with your doctor, who also looks at your family and your history. The sensible reading rule, then, is that a single LDL number without a risk profile says little. Place the result alongside your HDL, your triglycerides, your non-HDL cholesterol and your blood pressure, and assess it together with a doctor.

Adequate vitamin D levels are essential for strong bones, a well-functioning immune system, and overall well-being. Low levels may be associated with an increased risk of bone disorders, mood changes, and weakened immunity. Consult your healthcare provider for personalised advice.

Almost every page about HDL says the same thing: HDL is the good cholesterol, and the higher the better. Both halves of that sentence are wrong, which is exactly why this is the most important section on this page. <strong>Higher is not always better.</strong> The relationship between HDL and all-cause mortality is not a straight line but a U. In two large Danish population studies, together more than 116,000 men and women, the lowest mortality sat at an HDL of roughly 1.9 mmol/l in men and roughly 2.4 mmol/l in women. Above that, the curve turns: men with an HDL of 3.0 mmol/l or more had roughly twice the mortality, women from 3.5 mmol/l upwards around one and a half times. An extremely high HDL is therefore not a certificate of health, and it deserves a conversation with your doctor rather than congratulations. <strong>HDL is a gauge, not a dial.</strong> If a high HDL protects, then raising HDL ought to help. That has been tried extensively and it did not work. Drugs that inhibit the CETP transfer protein raised HDL by tens of percent and did not reduce heart attacks; the first in that class actually caused more deaths. Niacin raised HDL, but added no benefit on top of a statin and did add side effects. Genetic research points the same way: people who naturally carry a variant that raises HDL do not have a lower risk of myocardial infarction because of it, while that does hold for LDL-lowering variants. What does that mean? That a low HDL is not a cause, but a signal. HDL is low because something else is going on: visceral fat, insulin resistance, smoking, too little movement, or high triglycerides. Those are the factors that carry the risk. Fixating on the HDL number means treating the thermometer instead of the fever. <strong>So what do you do with it.</strong> Use HDL as context for the rest of your panel. A low HDL alongside high triglycerides and a raised fasting glucose together sketch a metabolic pattern that genuinely does carry risk. A low HDL also raises the cholesterol/HDL ratio, which is used in Dutch risk tables. But the values that predict risk most sharply are LDL, non-HDL cholesterol and ApoB, the number of risk-carrying particles. Your HDL says nothing about those. And finally: there is no target value for HDL. Your doctor does not set an HDL goal the way they set one for LDL, because no treatment has been shown to lower your risk by raising HDL.